By Topic

Analysis of Relationship between Apoptosis and Changes of Ca2+ in HepG-2 induced by CSA with laser scanning confocal technology

Sign In

Cookies must be enabled to login.After enabling cookies , please use refresh or reload or ctrl+f5 on the browser for the login options.

Formats Non-Member Member
$31 $13
Learn how you can qualify for the best price for this item!
Become an IEEE Member or Subscribe to
IEEE Xplore for exclusive pricing!
close button

puzzle piece

IEEE membership options for an individual and IEEE Xplore subscriptions for an organization offer the most affordable access to essential journal articles, conference papers, standards, eBooks, and eLearning courses.

Learn more about:

IEEE membership

IEEE Xplore subscriptions

2 Author(s)
Yu-bin Ji ; Center of Res. & Dev. on Life Sci. & Environ. Sci., Harbin ; Lei Yu

Laser scanning confoncal technology was used to study relationship between apoptosis and changes of Ca2+ induced by CSA (Capparis spinosa L. total alkaloid, CSA) on human heptocarcinoma cell HepG-2. Killing effects of CSA on human heptocarcinoma cell HepG-2 was measured by MTT method, while morphological observation on HepG-2 cells was completed by fluorescence microscope. Apoptosis of HepG-2 cells induced by CSA was measured by flow cytometry. In addition, change of intracellular Ca2+ level of CSA on HepG-2 cells was observed by laser scanning confocal microscope. Results: CSA had obvious cytotoxicity on HepG-2 in a dose-dependent manner, and its IC50 was 162.4 mug/ml. CSA could induce characteristic apoptosic morphology of HepG-2 cells, and apoptosis percentage was significantly higher than control one. Migration of cells cycle from S phase to G2 phase had been blocked by CSA. Concentration of Ca2+ in HepG-2 had been increased by CSA, which was positive correlation with drug dosage. CSA had obvious effects of killing and inducing apoptosis on human heptocarcinoma cell HepG-2, and overload of Ca2+ might be involved in the se events.

Published in:

Complex Medical Engineering, 2009. CME. ICME International Conference on

Date of Conference:

9-11 April 2009